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Iron potentiates nitric oxide scavenging by dithiocarbamates in tissue of septic shock mice.

Vanin and co-workers (Kubrina et al., Biochim. Biophys. Acta 1176 (1993) 240-244; Mikoyan et al., Biochim. Biophys. Acta 1269 (1995) 19-24) reported that short term (30 min) iron (Fe) exposure potentiates nitric oxide (NO) production in tissues of septic shock mice, based on increased formation of NO complex by diethyldithiocarbamate (DETC). We have reexamined the effect of Fe administration in mice treated with Escherichia coli lipopolysaccharide (LPS) and have not found any changes in nitrosylhemoglobin (HbNO) or (NOs- + NO3-) levels in blood 30 min after Fe-citrate complex injection. However, Fe-citrate promotes NO complex formation by iron-dependent NO traps: DETC, pyrrolidinedithiocarbamate (PDTC) and N-methyl-D-glucamine dithiocarbamate (MGD), when given simultaneously at 6 h after LPS. Rather than potentiation of NO production, our data support that short-term iron treatment (30 min) enhances in vivo spin trapping ability of dithiocarbamate.[1]


  1. Iron potentiates nitric oxide scavenging by dithiocarbamates in tissue of septic shock mice. Komarov, A.M., Mak, I.T., Weglicki, W.B. Biochim. Biophys. Acta (1997) [Pubmed]
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